Coronavirus SARS-COV-2 is able to find alternative ways of infection of human cells, even if there are no angiotensin-converting an ACE2 enzyme – a receptor that serves as a virus entry point in a cell. This was demonstrated by the University of Washington University in St. Louis and other US scientific organizations, whose article was published in Cell Reports magazine. Briefly about the study describes the press release on Phys.org.
An unexpected discovery was done when scientists have experienced various cancer cells of the lungs and upper respiratory tract with different levels of ACE2 expression on susceptibility to SARS-COV-2 coronaivirus. The researchers found that human adenocarcinoma cells H522, in which ACE2 is absent, susceptible to mutant form of coronavirus. To penetrate the cell, SARS-COV-2 typically uses a standard spike protein S, which interacts with ACE2, but in this case the mutant form of the S-protein virus is changed (this new mutation is denoted as E484D S). Classic, wild type of coronavirus is not able to infect cells H522.
Despite the mutation, Coronavirus E484D S remains susceptible to the antibodies in the blood serum of vaccinated patients, and the serum of the blood of passing people turned out to be less efficient. Although the receptor with which the mutant S-protein binds remains not known, scientists have found that the infection is blocked if the cell has a deficiency of heparasulfates – proteins with polysaccharide residues that are near the cell membrane and are most likely associated with an unknown receptor.
scientists were sequenced by a transcript of H522 infected cells infected with Coronavirus to understand what was happening with cells when infected. The transcript is a combination of all RNA molecules that are directly produced by gene activity and either participate in the synthesis of proteins encoded by genes or carry out regulatory functions. The researchers followed changes in the transcript for four days of infection, noting the growth of replicated viral RNA, and 5-10 percent of the entire cell RNA accounted for its share in the peak of infection. In addition to the virus RNA, the levels of viral proteins and immune proteins also grew up, including interferon gamma.